Neurology- Neurophatology Flashcards
(49 cards)
Common brain lesions
- Frontal lobe
- Frontal eye fields
Disinhibition and deficits in concentration, orientation, judgment; primitive reflexes.
Eyes look toward (destructive) side of lesion. In seizures (irritative), eyes look away from side of the lesion.
Common brain lesions
- Paramedian pontine reticular formation
- Medial longitudinal fasciculus
Ipsilateral gaze palsy (inability to look toward side of lesion).
Internuclear ophthalmoplegia (impaired adduction of ipsilateral eye; nystagmus of contralateral eye with abduction).
Common brain lesions
- Dominant parietal cortex
- Nondominant parietal cortex
Agraphia, acalculia, finger agnosia, left-right disorientation (Gestmann Sx).
Agnosia of the contralateral side of the world. (Hemispatial neglect syndrome)
Common brain lesions
- Hippocampus (bilateral)
- Basal ganglia
- Subthalamic nucleus
Anterograde amnesia
May result in tremor at rest, chorea, athetosis.
Contralateral hemiballismus
Common brain lesions
- Mammillary bodies (bilateral)
Wernicke-Korsakoff syndrome—Confusion, Ataxia, Nystagmus, Ophthalmoplegia, memory loss, confabulation, personality changes.
Common brain lesions
- Amygdala (bilateral)
- Dorsal midbrain
Klüver-Bucy syndrome—disinhibited behavior (HSV-1 encephalitis)
Parinaud syndrome—vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus. (Stroke, hydrocephalus, pinealoma)
Common brain lesions
- Reticular activating system (midbrain)
- Cerebellar hemisphere
- Cerebellar Vermis
Reduced levels of arousal and wakefulness (eg, coma).
Intention tremor, limb ataxia, loss of balance; ipsilateral deficits; fall toward side of lesion.
Truncal ataxia (wide-based, “drunken sailor” gait), dysarthria.
Common brain lesions
- Decorticate (flexor) posturing
- Decerebrate (extensor) posturing
lesion above red nucleus, presents with flexion of upper extremities and extension of lower extremities.
Lesion at or below red nucleus, presents with extension of upper and lower extremities.
Ischemic brain disease/stroke
- Most vulnerable areas
- Stroke imaging
hippocampus, neocortex, cerebellum (Purkinje cells), watershed areas.
Noncontrast CT to exclude hemorrhage (before tPA can be given). CT detects ischemic changes in 6–24 hr. Diffusion-weighted MRI can detect ischemia within 3–30 min.
Ischemic stroke
- Types
- Treatment
Thrombotic, embolic, hypoxic
tPA (if within 3–4.5 hr). Medical therapy (eg, aspirin, clopidogrel); optimum control of blood pressure, blood sugars, lipids; and treat conditions that risk (eg, atrial fibrillation, carotid artery stenosis).
Neonatal intraventricular hemorrhage
Bleeding into ventricles. Increased risk in premature and low-birth-weight infants. Originates in germinal matrix, a highly vascularized layer within the subventricular zone.
Due to reduced glial fiber support and impaired autoregulation of BP in premature infants. Can present with altered level of consciousness, bulging fontanelle, hypotension, seizures, coma.
Intracranial hemorrhage
- Epidural
Rupture of middle meningeal artery (pterion).
Scalp hematoma and rapid intracranial expansion under systemic arterial pressure transtentorial
herniation, CN III palsy.
CT shows biconvex (lentiform), hyperdense blood collection
Intracranial hemorrhage
- Subdural
Rupture of bridging veins. Seen in shaken babies. Predisposing: brain atrophy, Trauma.
Crescent-shaped hemorrhage that crosses suture lines. Can cause midline shift, findings of “acute on chronic” hemorrhage.
Intracranial hemorrhage
- Subarachnoid hemorrhage
Bleeding due to trauma, or rupture of an aneurysm, or arteriovenous malformation. Patients complain of “worst headache of my life.”
Xanthochromic spinal tap. Vasospasm can occur due to
blood breakdown or rebleed 3–10 days after hemorrhage ischemic infarct; nimodipine used to prevent/reduce vasospasm.
Intracranial hemorrhage
- Intraparenchymal hemorrhage
by systemic hypertension. Also seen with amyloid
angiopathy. vasculitis, neoplasm. May be 2º to reperfusion injury in ischemic stroke.
Hypertensive hemorrhages (Charcot- Bouchard microaneurysm) most often occur in putamen of basal ganglia (lenticulostriate vessels), followed by thalamus, pons, and cerebellum.
Effects of strokes
Pag. 498, 499
Diffuse axonal injury
Caused by traumatic shearing forces during rapid acceleration and/or deceleration of the brain.
devastating neurologic injury, often causing coma or
persistent vegetative state
Lateral medullary (Wallenberg) syndrome
Nucleus ambiguus effects are specific to PICA lesions.
“Don’t pick a (PICA) horse (hoarseness) that can’t eat
(dysphagia).”
Also supplies inferior cerebellar peduncle (part of cerebellum).
Lateral pontine syndrome
Facial nucleus effects are specific to AICA lesions.
“Facial droop means AICA’s pooped.”
Also supplies middle and inferior cerebellar peduncles (part of cerebellum).
aphasias
higher-order language deficit (inability to understand/produce/use language appropriately)
Pag. 500
Saccular aneurysm (berry)
Occurs at bifurcations in the circle of Willis. Most common site is junction of ACom and ACA. Associated with ADPKD, Ehlers-Danlos syndrome.
Usually clinically silent until rupture subarachnoid hemorrhage focal neurologic deficits
Saccular aneurysm (berry)
- ACom
- MCA
- PCom
Bitemporal hemianopia; ischemia in ACA distribution contralateral lower extremity hemiparesis, sensory deficits.
Ischemia in MCA distribution contralateral upper extremity and lower facial hemiparesis, sensory deficits.
Ipsilateral CN III palsy mydriasis (“blown pupil”); may also see ptosis, “down and out” eye
Partial (focal) seizures
- Types
Simple partial (consciousness intact)—motor, sensory, autonomic, psychic
Complex partial (impaired consciousness,
automatisms)
Generalized seizures
- Types
Absence (petit mal)—3 Hz spike-and-wave discharges, no postictal confusion, blank stare
Myoclonic—quick, repetitive jerks
Tonic-clonic (grand mal)—alternating stiffening and movement
Tonic—stiffening
Atonic—“drop” seizures (falls to floor); commonly mistaken for fainting
